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Assessment of Morphine-induced Hyperalgesia and Analgesic Tolerance in Mice Using Thermal and Mechanical Nociceptive Modalities
Published on: July 29, 2014
Brain catecholamines and adrenocortical activation by morphine in the cat
1Instituto de Endocrinología 'Gregorio Marañón', Centro de Investigaciones Biológicas, C.S.I.C., Madrid, Spain.
Neuroscience Letters
|July 17, 2009
Summary
Alpha-methyl-p-tyrosine (H 44/68) increases plasma cortisol in cats, independent of catecholamine synthesis impairment. Morphine may elevate ACTH secretion by increasing noradrenaline turnover.
Area of Science:
- Neuroendocrinology
- Pharmacology
Background:
- The relationship between catecholamine synthesis and the pituitary-adrenal axis is complex.
- Opioids are known to influence both central neurotransmitter systems and hormonal regulation.
Purpose of the Study:
- To investigate the effect of alpha-methyl-p-tyrosine (H 44/68) on plasma cortisol and diencephalic noradrenaline in cats.
- To explore the interaction between H 44/68, morphine, and the pituitary-adrenal system.
Main Methods:
- Administration of alpha-methyl-p-tyrosine (H 44/68) at 250 mg/kg to adult cats.
- Measurement of plasma cortisol levels.
- Assay of noradrenaline content in the diencephalon.
- Co-administration of H 44/68 and morphine.
Main Results:
- H 44/68 administration led to increased plasma cortisol prior to decreased diencephalic noradrenaline.
- Morphine, when administered with H 44/68, appeared to increase noradrenaline turnover.
- These findings suggest H 44/68-induced ACTH release may be independent of catecholamine synthesis inhibition.
Conclusions:
- The mechanism of H 44/68-induced ACTH release in cats may not directly depend on catecholamine synthesis impairment.
- Morphine's effect on ACTH secretion could be linked to its influence on noradrenaline turnover in the brain.
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